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Time course of the inflammatory and oxidative stress response to pulmonary infection in mice
Matthias Lange1, Yoshimitsu Nakano, Daniel L Traber
1Department of Anesthesiology, Investigational Intensive Care Unit, The University of Texas Medical Branch and Shriners Hospitals for Children, Galveston, Texas 77550, USA. lanm@gmx.de
Abstract:
The pathophysiological response to pulmonary infection includes a surge of proinflammatory cytokines and excessive production of nitric oxide (NO), but the time changes are not sufficiently defined. The current study was designed to assess the time course of proinflammatory cytokines and NO production in a murine model of pulmonary infection. The injury was induced by intranasal administration of live Pseudomonas aeruginosa (3.2 × 10(7) colony-forming units) in C57BL/6 wild-type mice. The animals were euthanized at 3, 6, 9, 12, and 15 hours postinjury. Additional mice received sham injury (0 hours; control). Lung tissue and plasma samples were harvested at the respective time points. The injury induced an early increase in interleukin (IL)-1 β protein in lung tissue that persisted during the entire study period with a peak at the 9-hour time point. The increases in TNF-α and IL-6 proteins in lung tissue were less intense, but showed a peak about 9 hours postinjury. The plasma levels of IL-1 β and tumor necrosis factor (TNF)-α protein were not elevated during the experimental period, but only an increase in plasma levels of IL-6 plasma protein was detected. These findings compensate for the limitations of previous experiments with similar infection models and improve the understanding of pathophysiologic alterations in response to pulmonary infection. In addition, the identification of the time changes of the described pathogenetic factors may enhance the timing of innovate therapeutic approaches in future experiments.
Insights
Pulmonary infection triggers early increases in lung interleukin-1 beta, tumor necrosis factor-alpha, and interleukin-6. These inflammatory markers peak around 9 hours, aiding understanding of infection dynamics.
Area of Science:
- Immunology
- Pathophysiology
- Microbiology
Background:
- Pulmonary infections involve inflammatory responses, including cytokine surges and nitric oxide (NO) production.
- The precise temporal dynamics of these responses are not fully understood.
- Pseudomonas aeruginosa is a common cause of hospital-acquired pneumonia.
Purpose of the Study:
- To investigate the time course of proinflammatory cytokines and NO in a murine model of pulmonary infection.
- To establish a detailed timeline of key inflammatory mediators following Pseudomonas aeruginosa challenge.
Main Methods:
- C57BL/6 wild-type mice were infected intranasally with Pseudomonas aeruginosa.
- Lung tissue and plasma samples were collected at 3, 6, 9, 12, and 15 hours post-infection.
- Levels of interleukin (IL)-1β, tumor necrosis factor-alpha (TNF-α), and IL-6 were measured.
Main Results:
- Lung IL-1β protein increased early and persisted, peaking at 9 hours post-infection.
- Lung TNF-α and IL-6 showed less intense increases, also peaking around 9 hours.
- Plasma IL-1β and TNF-α remained unchanged, while plasma IL-6 showed a detectable increase.
Conclusions:
- This study defines the temporal profiles of key inflammatory cytokines in response to Pseudomonas aeruginosa lung infection.
- Understanding these time-dependent changes offers insights into infection pathophysiology.
- The findings may inform the timing of future therapeutic interventions for pulmonary infections.
